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• W2332921189 abstract "Objective: To evaluate the antioxidant potential of Laquinimod, a novel oral therapeutic for the treatment of Multiple Sclerosis (MS). Background MS is an inflammatory autoimmune disorder, where chronic disability is due to axonal and neuronal degeneration, which is not accessible to conventional therapy and linked to oxidative stress. Laquinimod is an orally administered CNS-active immunomodulator. Phase III data in RRMS patients showed beneficial effects of laquinimod on clinical disease activity as evidenced by slowing the progression of disability, reducing the rate of MRI-measured brain volume loss and reducing relapse rates, all coupled with a favorable safety and tolerability profile. Design/Methods: We investigated the role of laquinimod in oxidative stress using hippocampal HT22 cells. In these cells, extracellular glutamate blocks cystine import via the glutamate/cystine-antiporter system Χc. Lack of intracellular cystine leads to glutathione depletion and cell death due to oxidative stress. Protection in this model was previously shown to be mediated by the transcription factors ATF4, CREB, NRF2 or SRF. We measured cell survival, concentration and time dependence, total cellular glutathione content, and the induction of antioxidant proteins by quantitative real-time PCR and transcriptional activation by dual-luciferase experiments. Results: Laquinimod robustly protected against glutamate toxicity, inhibition of γ-glutamylsynthetase, and direct oxidative stress induced by hydrogen peroxide without elevating basal intracellular glutathione levels. Protection was time-dependent and took seven days to develop. We observed a relevant effect on the expression of glutamate cysteine ligase and xCT, the functional unit of system Χc. Conclusions: Laquinimod protects hippocampal HT22 cells from oxidative stress. This protection takes seven days to develop, which hints to mechanism involving changes in gene transcription not mediated by NRF2. These results suggest transcriptional activation by other transcription factors, which are currently investigated by dual luciferase experiments using promoters of glutamate cysteine ligase and xCT. Supported by: TEVA. Disclosure: Dr. Methner has nothing to disclose. Dr. Albrecht has received research support from Novartis. Dr. Bouchachia has nothing to disclose. Dr. Hartung has received personal compensation for activities with Bayer Pharmaceuticals Corporation, Biogen Idec, BioMS, Genzyme Corporation, Merck Serono, Novartis, Sanofi-Aventis and Teva as a speaker and/or consultant." @default.
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• W2332921189 date "2012-04-22" @default.
• W2332921189 modified "2023-09-26" @default.
• W2332921189 title "Prolonged Incubation with Laquinimod Protects Hippocampal Cells from Oxidative Stress (P02.110)" @default.
• W2332921189 doi "https://doi.org/10.1212/wnl.78.1_meetingabstracts.p02.110" @default.
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